Evidence map›Paper›PMID 23555285›Full record

ArticlePLoS genetics2013

Long noncoding RNA MALAT1 controls cell cycle progression by regulating the expression of oncogenic transcription factor B-MYB.

Vidisha Tripathi, Zhen Shen, Arindam Chakraborty, Sumanprava Giri, Susan M Freier, Xiaolin Wu, Yongqing Zhang, Myriam Gorospe, Supriya G Prasanth, Ashish Lal and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 450 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
450citing papers in PubMed, 1 pooled it
26.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

450 citing papers in PubMed, 1 synthesis or guideline pooled it, 770 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026
    Review
  4. Global deletion ofbioRxiv : the preprint server for biology · 2026
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390 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 1 country.

Vidisha TripathiDepartment of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Zhen Shen
Arindam Chakraborty
Sumanprava Giri
Susan M Freier
Xiaolin Wu
Yongqing Zhang
Myriam Gorospe
Supriya G Prasanth
Ashish Lal
Kannanganattu V Prasanth
University of Illinois Urbana-Champaign · USNational Institute on Aging · USFrederick National Laboratory for Cancer Research · USIonis Pharmaceuticals (United States) · USNational Institutes of Health · US

Funding

Influence of Post-transcriptional Gene Regulation on Cell Senescence and AgingZIAAG000393 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$24.1M
Characterization of nuclear retained RNA-mediated gene regulatory mechanismR01GM088252 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KANNANGANATTU, PRASANTH KUMAR VIJAYAN · 2011 to 2015
$1.4M
Role of ORCA in DNA replicationR01GM099669 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI PRASANTH, SUPRIYA G · 2012 to 2016
$1.3M
NIGMS NIH HHS NIH GM088252NIGMS NIH HHS NIH GM099669NIGMS NIH HHS R01 GM088252NIGMS NIH HHS R01 GM099669
6 · The paper itself

Abstract

The long noncoding MALAT1 RNA is upregulated in cancer tissues and its elevated expression is associated with hyper-proliferation, but the underlying mechanism is poorly understood. We demonstrate that MALAT1 levels are regulated during normal cell cycle progression. Genome-wide transcriptome analyses in normal human diploid fibroblasts reveal that MALAT1 modulates the expression of cell cycle genes and is required for G1/S and mitotic progression. Depletion of MALAT1 leads to activation of p53 and its target genes. The cell cycle defects observed in MALAT1-depleted cells are sensitive to p53 levels, indicating that p53 is a major downstream mediator of MALAT1 activity. Furthermore, MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing. In human cells, MALAT1 promotes cellular proliferation by modulating the expression and/or pre-mRNA processing of cell cycle-regulated transcription factors. These findings provide mechanistic insights on the role of MALAT1 in regulating cellular proliferation.

Indexed as

NeoplasmsRNA, Long NoncodingAlternative SplicingCell Cycle CheckpointsCell Cycle ProteinsCell ProliferationGene Expression Regulation, NeoplasticHumansOligonucleotide Array Sequence AnalysisRNA PrecursorsTrans-ActivatorsTranscriptional ActivationTumor Suppressor Protein p53Cell Cycle ProteinsMALAT1 long non-coding RNA, humanMYBL2 protein, humanRNA, Long NoncodingRNA PrecursorsTP53 protein, humanTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID23555285
PMCPMC3605280
OpenAlexW2087528029

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.